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Our work examines the molecular basis of plant disease resistance. The plant immune system includes many elements that are unique to plants. We study disease resistance in part because host-pathogen dynamics and the molecular workings of immune systems are fascinating biological topics. On a more practical level, one of the best ways to control plant diseases is by genetically determined resistance. Genetic resistance is convenient for the grower and minimizes the need for costly, time-consuming and/or potentially toxic external treatments. Plant breeders and their predecessors have utilized genetically determined plant disease resistance for literally thousands of years, but the molecular basis of this resistance is only partly understood. We work to identify and study the genes and the biochemical/cellular processes that control pathogen recognition, defense signal transduction, and the execution of successful resistance responses. We seek to expand our basic understanding of plant interacations with pathogens, and expect that some of this work will contribute to the development of plants with improved disease resistance.

Our research often utilizes Arabidopsisthaliana because of the extraordinary experimental versatility of this plant species. We also study soybean, the most abundant legume crop and a major contributor to world food supplies. Other plant species are studied as the need arises. We work with many different pathogens, but primarily with the bacterial blight pathogen Pseudomonassyringaepv. tomato and with soybean cyst nematode (Heterodera glycines).

Soybean cyst nematode is the most economically damaging pathogen of soybean worldwide. We are uncovering the molecular mechanisms that underpin the function and evolution of soybean Rhg1, a genetic locus that is heavily utilized by farmers to control SCN disease. We found that three distinct gene products encoded at Rhg1 contribute to SCN resistance. We also found that a striking form of copy number variation is present at Rhg1 (up to ten tandem repeats of a 31.2kb genome segment encoding those three distinct gene products). We are studying the mechanisms of this Rhg1-mediated resistance, and we are also studying other genes and processes that contribute to SCN resistance.

We discovered that poly(ADP-ribosyl)ation plays significant roles in plant responses to infection and are now studying the plant-microbe interaction processes where poly(ADP-ribosyl)ation is relevant, including plant genome stability. We recently discovered that microbial pathogens can activate damage of plant host DNA early in the infection process, and we are now studying how this damage arises and how plant immune responses mediate protection/preservation of genetic information.

We are developing ways to identify and manipulate LRR active sites within plant disease resistance proteins and other LRR proteins. The flagellin receptor FLS2 of Arabidopsis has been our primary model. We are working to understand how ligand specificity is determined, and how it can be altered in a targeted way by in vitro evolution. We have also examined other aspects of receptor activation, and the ways in which some bacterial pathogens have evolved to escape plant detection of their flagellins.